Amyloidosis in Captive Cheetahs – Is it in Their Genes?

Cheetahs in captivity have an unusually high prevalence of a fatal disease called systemic amyloid A (AA). Amyloid is a protein that forms in the bloodstream during inflammation and deposits in organs throughout the body. These proteins accumulate over time in organs such as the liver, spleen, heart, and kidneys, ultimately progressing to organ failure. The kidneys are particularly affected in cheetahs, which typically leads to renal dysfunction and renal failure in captive animals. Curiously, wild cheetahs are virtually unaffected by this disease process.

Smithsonian Conservation Biology Institute scientists Ashley Franklin and Adrienne Crosier, in partnership with the cheetah Species Survival Plan, pathologist Karen Terio, scientists at the University of Maryland College Park and Drs. Anne Schmidt-Küntzel and Laurie Marker of the Cheetah Conservation Fund in Namibia, recently analyzed the systemic amyloid A of cheetahs to determine what effect genetics plays in the incidence of this disease.

Scientists determined that the there was a genetic influence on the level of serum amyloid A, but that other factors had an even bigger influence. There was also no link between the genetic variant carried and diseases status, suggesting that the amyloidosis found in captive cheetahs is not inherited, but rather secondary to chronic inflammation.

Chronic gastritis of varying degrees is present in virtually all captive cheetahs for reasons yet to be fully understood, though it is thought to be associated with environmental factors and stress. In this analysis, amyloidosis was found to be very common in animals known to have moderate to severe gastritis, leading the scientists to conclude that the high prevalence of systemic amyloid A amyloidosis in captive cheetahs is more likely the result of chronic inflammation and/or other environmental factors rather than their genes.

Studies help us gain insights into diseases that uniquely and profoundly impact the cheetah’s survival in captivity. With a better understanding of the factors that cause amyloidosis, we can better manage, treat, and find ways to prevent the disease that affects so many of our vital and valuable captive animals.

Diagram of AA amyloid formation and the potential prion-like transmission of AA amyloidosis by fecal shedding and oral uptake of the amyloid. The photo shows an example of Congo red-stained AA amyloid fibril deposits in hamster liver tissue (courtesy of John Coe, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases).

Infographic from Proceedings of the National Academy of Sciences (PNAS) vol. 105 no. 20 > Byron Caughey, 7113–7114 Are cheetahs on the run from prion-like amyloidosis?